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Effect of duodenal switch procedure on gastric acid production, intragastric pH, gastric emptying, and gastrointestinal hormones.

The duodenal switch operation preserves the pylorus and the proximal 3 to 7 cm of duodenum in continuity with the stomach while diverting pancreaticobiliary secretions. We compared it with the Roux-en-Y without vagotomy or antrectomy in 12 dogs with innervated gastric pouches. Acid secretion was inhibited between tests using ranitidine in the Roux-en-Y group only, but two of the six dogs still developed stomal ulcers and the remainder showed stomal hyperemia. This may be due to a significant increase in gastric acid output after Roux-en-Y, but gastric emptying and plasma gastrin, cholecystokinin, secretin, gastric inhibitory polypeptide, peptide YY, and neurotensin were similar after both procedures. In 12 patients and a further 6 dogs, the duodenal switch caused no significant change in the intragastric pH environment as assessed by intragastric pH monitoring. The duodenal switch is a suitable procedure for pancreaticobiliary diversion.

Anastomosis, Roux-en-Y↗

Effect of Ca2+, Mg2+, NaN3, cholinergic agents, and gastrointestinal hormones on the guanylate cyclase from guinea pig gastric mucosa.

Guanylate cyclase in the guinea pig fundic mucosa occurred in two enzymatic forms: a "soluble" form and a particulate form. The mean basal activity of the soluble fraction measured in the presence of 300 micrometer guanosine-5'-triphosphate and 5 mM MnCl2 was 72.6 +/- 5.3 pmoles of cyclic GMP per mg of protein per min. Guanylate cyclase activity was dependent on Mn2+; it was increased by sodium azide (NaN3), CaCl2, cysteine, secretin, and cholecystokinin, but it was not influenced by gastrin, histamine, cholinergic esters, prostaglandins E1 and A1. NaN3 (1 mM) decreased the apparent Km for MnCl2 and potentiated the effects of MgCl2. The activity of the particulate fraction represented about 14% of that of the supernatant fraction. The guanylate cyclase activity of that fraction was not modified by NaN3, gastrin, cholinergic agents, secretin, or cholecystokinin. Cysteine inhibited its activity. These data do not support the hypothesis that cyclic GMP acts as a second messenger for the action of cholinergic agents and gastrin in the guinea pig gastric mucosa.

Animals↗

Effects of carbohydrate type on postprandial blood pressure, neuroendocrine and gastrointestinal hormone changes in the elderly.

Previous studies have demonstrated that blood pressure falls postprandially in fit elderly subjects, the greatest changes occurring after meals with a high carbohydrate content. To evaluate the influence of the type of carbohydrate on postprandial blood pressure, the effects of equivalent energy content (2.4 MJ) high complex (starch) and high simple (monosaccharide) carbohydrate meals were studied in seven healthy elderly subjects. Blood pressure, heart rate, autonomic function, plasma catecholamines, insulin and neurotensin levels were measured pre- and postprandially. Greater falls in supine and erect systolic blood pressure occurred after the high simple than the high complex carbohydrate meal (p less than 0.05). No differences were found in supine or erect diastolic blood pressure, heart rate or in any of the biochemical parameters measured between the meal types. It is concluded that a simple carbohydrate meal results in a greater postprandial fall in blood pressure than an equivalent energy complex carbohydrate meal in the elderly, although the mechanisms for these changes are unknown.

Aged↗

Pancreatic trophism following colectomy in rats: the potential role of gastrointestinal hormones.

It has been shown that the large bowel contains substances with a potential to inhibit exocrine pancreatic function. Following large bowel removal in rats, there is an increase of pancreatic weight, digestive enzyme concentration, and secretion capacity in vitro. To evaluate the role of various GI hormones in the exocrine pancreatic adaptation following colectomy, we measured plasma cholecystokinin (CCK), neurotensin, glucagon, and insulin after meal stimulation. The test meal was applied via a transabdominal gastric tube in eight colectomized Wistar rats after a median of 18 days following surgery. Ten rats with a gastric tube without previous bowel surgery served as controls. After large bowel removal, there was impaired glucose tolerance and attenuated plasma insulin secretion. Baseline plasma glucagon levels were increased after colon removal, whereas the total postprandial glucagon release was decreased. Baseline and postprandial neurotensin values were comparable in both the experimental and control animals. Baseline and postprandial CCK plasma levels were intensely increased in the colectomized rats. It is assumed that the baseline and postprandial CCK pattern in rats after subtotal colectomy is responsible for exocrine pancreatic adaptation.

Animals↗

[Interaction between gastrointestinal hormones and endocrine regulation].

The vicinity of several hormone-producing glands as part of the anatomy of the intestinal tract and the resulting interaction has been confirmed by the discovery of hormonal factors of a specifically gastro-intestinal origin. Today we are mainly interested in the interaction between intermediary metabolism and incretory intestinal function; this is characterized by the joint action of conventional glandular hormones such as insulin and pancreatic glucagon as well as by the incretion of diffuse intestinal organs, hormones such as secretin, pancreozymin, motilin, VIP and GIP. The latter are at present subject of active research with the object of discovering their physiological significance be it as tissue hormones or as humoral agents with a "long distance" impact; their role within pathophysiology is also of interest. GIP ("gastric inhibitory peptide"), apart form acting upon the intestinal tract, also causes a marked rise in insulin production; this GIP possibly is the factor responsible for the difference in glucose tolerance following i. v. or oral administration of glucose, something that scientists have been trying to discover for a long time. We have also endeavored to investigate somatostatin. This substance was originally discovered as a hypothalamic factor with inhibitory action on growth hormone secretion; in the meantime, however, cells containing and possibly also producing somatostatin have also been detected in the intestine and particularly in the islets of Langerhans (D-cells). Since somatostatin inhibits insulin secretion and especially glucagon release as well as the exretory functions of the stomach and of the pancreas, the significance of this hormone possibly is that of a tissue hormone with inhibitory action on adjacent cells. As factor inhibiting both endocrine and exocrine secretory processes it would combine these two complexes. The possible therapeutic significance of somatostatin administration to diabetics would lie in the saving of insulin. A third sector of present-day research deals with the interaction between the calcium metabolism and the hormones involved as well as the intestine. We know that patients suffering from primary hyperparathyroidism are prone to contract stomach ulcers and pancreatitis; patients with a gastrinoma and a hyperfunction of the epithelial bodies suffer from a Zollinger-Ellison-sindrome and this again suggests association with endocrine polyadenomatosis (Wermer syndrome). The inhibitory action of the parathormone antagonist calcitonin on the exocrine functions of the intestinal tract, such as the acid secretion of the stomach and the enzyme secretion of the pancreas, have already given rise to some considerations and experiments relative to treatment. It is to be hoped that because of all the joint observations cited above there will be better intergration of research both from the aspect of gastro-enterology and endocrinology. This might hopefully elucidate some of the unresolved problems ranging from basic research to practical application.

Adolescent↗

Cyclic AMP in pancreatic acinar cells: effects of gastrointestinal hormones.

In the presence of 5 mM theophylline, secretin and vasoactive intestinal peptide (VIP) each increased cyclic adenosine 3':5'-monophosphate (cyclic AMP) in acinar cells isolated from guinea pig pancreas. Without theophylline, neither peptide altered cellular cyclic AMP. Glucagon, which is similar to secretin and VIP both in chemical structure and spectrum of biologic activities, neither stimulated cellular cyclic AMP nor inhibited the stimulation produced by secretin or by VIP. Other agents which were tested and found not to increase cellular cyclic AMP were cholecystokinin, carboxyl-terminal octapeptide of cholecystokinin, gastrin I, gastrin II, bovine pancreatic polypeptide, carbamylcholine, and prostaglandin E1. Neither carboxyl-terminal octapeptide nor gastrin I altered the stimulation of cellular cyclic AMP produced by secretin or VIP. With natural secretin a significant increase in cellular cyclic AMP could be detected at concentrations as low as 3 x 10(-10) M and maximal stimulation occurred at 10(-8) M. VIP was approximately 1% as potent as natural secretin and maximal concentrations of secretin plus VIP increased cellular cyclic AMP to the same value as was obtained with a maximal concentration of secretin alone.

Animals↗

[Effects of thread embedding therapy on nucleotides and gastrointestinal hormones in the patient of chronic gastritis].

OBJECTIVE: To observe therapeutic effect of thread embedding therapy on chronic gastritis. METHODS: Seventy cases of chronic gastritis were randomly divided into the treatment group (n = 36) treated by thread embedding therapy and the control group (n = 34) by acupuncture. Weishu (BL 21), Zhongwan (CV 12) and Zusanli (ST 36) were selected as main points. And plasma contents of cAMP, cGMP, gastrin and substance P were observed before and after treatment. RESULTS: The total effective rate was 88.89% in the treatment group and 76.47% in the control group with a significant difference between the two groups (P < 0.05); there were significant differences before and after treatment in plasma contents of cAMP, cGMP, gastrin and substance P in the two groups (P < 0.01), and the changes of these indexes in the treatment group were significantly superior to the control group (P < 0.05). CONCLUSION: Thread embedding therapy has a definite therapeutic effect on chronic gastritis and it can adjust nucleotides, gastrin and substance P to improve the functions of the nerve-endocrine-immunity network.

Acupuncture Points↗

Regulation of food intake by gastrointestinal hormones.

PURPOSE OF REVIEW: Complex physiological mechanisms have evolved to control food intake in mammals, which in health ensure the relative stability of body weight in adults. Central brain centres, gut-derived peptides and adipose-derived signals result in an integrative response to defend against starvation. Enteroendocrine cells throughout the gut and pancreas secrete a number of peptides with activity on gut motility, gut secretions and appetite. Understanding the interactions between different gut peptides has produced a rewardingly active research field with many unanswered questions. RECENT FINDINGS: Many gut peptides are now in translational research programmes to investigate their potential in human physiology and disease. Ghrelin has been shown in short-term human studies to both increase appetite and body weight. Oxyntomodulin has been shown to reduce weight and food intake in a 4 week study in humans. Anorectic activity of peptide YY(3-36) has been confirmed in a number of animal models. Obestatin has been identified as a novel gut peptide. Increasing evidence points to the effect of gastric-bypass surgery on body weight, including alteration of gut peptide activity. SUMMARY: Gut peptides, or gut-peptide mimetics, show great promise for use as therapeutic agents for the treatment of obesity and cachexia.

Animals↗

Effect of gastrointestinal hormones and synthetic analogues on the growth of pancreatic cancer.

The effects of hormones and synthetic analogues have been examined on the growth of 2 human pancreatic cancer cell lines, MiaPaCa2 a well-established cell line and PANI which was derived in our own laboratories from a tumour specimen. The hormones/growth factors included gastrin (G-17), epidermal growth factor (EGF) and bombesin, while the synthetic analogues used were a gastrin receptor antagonist (CR 1718), a somatostatin analogue (RC-160) and a bombesin receptor antagonist (ICI 216,140). Cell proliferation was assessed by the [75Se]selenomethionine uptake method which has been shown to correlate with cell counts. The effect of each hormone or growth factor on growth was expressed as a percentage of the untreated control. There were 5 replicates in each experiment, and each one was repeated at least 3 times. In vitro growth of both cell lines was unaffected by gastrin, bombesin or the respective antagonists (CR1718 and ICI 216140). The somatostatin analogue RC-160 also had no effect on basal growth. Significant growth stimulation of both MiaPaCa2 and PANI was seen with epidermal growth factor. We tested the hypothesis that somatostatin analogues may inhibit EGF-stimulated growth on both MiaPaCa2, a somatostatin receptor positive cell line, and on PANI which is negative for somatostatin receptors. RC-160 did not inhibit EGF-stimulated growth of either MiaPaCA2 or PANI. Both cell lines were established in vivo as xenografts in nude mice. The effect of RC-160 on tumour growth was measured. RC-160 inhibited the growth of MiaPaCa2, the somatostatin receptor-positive cell line, but not of PANI.

Adenocarcinoma↗

Effect of gastrointestinal hormones on choleresis from the isolated perfused rat liver.

Using isolated perfused rat liver, the direct effect of secretin, glucagon, caerulein, insulin and somatostatin on choleresis was investigated. When the liver was perfused in the absence of sodium taurocholate, the bile volumes were: control, 0.33 +/- 0.01 (mean +/- S.E.M.) ml/10 g liver per 50 min; secretin 0.05 U/ml, 0.39 +/- 0.01 (P less than 0.01); glucagon 10(-10) M, 0.44 +/- 0.02 (P less than 0.01); caerulein 10(-8) M, 0.34 +/- 0.03 (n.s.); insulin 1 mU/ml, 0.35 +/- 0.02 (n.s.); glucagon plus somatostatin 10(-7) M, 0.46 +/- 0.03 (n.s. vs. glucagon alone), respectively. When 10(-5) M sodium taurocholate was present in the perfusate, the bile volumes were: control, 0.61 +/- 0.03; secretin, 0.63 +/- 0.01 (n.s.); glucagon, 0.70 +/- 0.01 (P less than 0.05); caerulein, 0.55 +/- 0.01 (n.s.); insulin, 0.62 +/- 0.04 (n.s.); somatostatin, 0.59 +/- 0.01 (n.s.); respectively. Glucagon increased glucose output and cyclic AMP in the effluent from the liver neither of which were suppressed by somatostatin. Secretin increased cyclic AMP but not glucose output. These results indicate that glucagon has the most potent action on bile acid-independent canalicular bile, that caerulein and insulin do not act on canalicular bile production directly and that somatostatin does not directly suppress canalicular bile production nor hepatic glucose output produced by glucagon in rats.

Animals↗

Effects of vagotomy on satiety induced by gastrointestinal hormones in the rat.

Cholecystokinin, bombesin and pancreatic polypeptide are all reported to induce satiety in rodents. To test the hypothesis that cholecystokinin and bombesin induce satiety through release of pancreatic polypeptide, we compared the satiety inducing properties of each peptide in rats trained to eat a liquid diet (Magnacal). Studies were repeated after transabdominal truncal vagotomy (n = 8) or sham operation (n = 8). Peptides were given by intraperitoneal injection, and the volume of Magnacal ingested over a 2 hr period measured. After the injection of saline, unoperated rats (n = 16) ingested 30 +/- 2.3 ml of Magnacal. Caerulein (9 nmol/kg) and bombesin (27 nmol/kg) significantly inhibited food intake to 8 +/- 2.5 ml and 20 +/- 2.1 ml respectively. In contrast pancreatic polypeptide (27 nmol/kg) had no significant effect on food intake. Both caerulein and bombesin retained the ability to reduce food intake after vagotomy although the effects of caerulein were somewhat blunted. No significant changes in serum pancreatic poly peptide concentrations were observed after either the caerulein or bombesin injection. As both peptides release pancreatic polypeptide in higher mammals, species differences in release mechanisms appear to exist. We would conclude that caerulein and bombesin induced satiety is independent of pancreatic polypeptide release and that the weight loss induced by pancreatic polypeptide in obese rodents is unlikely to be due to induction of satiety.

Animals↗

In vitro interactions of gastrointestinal hormones on cyclic adenosine 3':5'-monophosphate levels and amylase output in the rat pancreas.

Four-fold increases in cyclic AMP levels were observed 5 to 10 min after rat pancreatic fragments were incubated with 10-7 M secretin or 10-6 M vasoactive intestinal polypeptide (VIP), in addition to 10 mM theophylline. From dose-response curves it appears that, on a molar basis, the potency of secretin was 20 times higher than that of VIP. It is concluded that cyclic AMP is probably the intracellular messenger of both secretin and VIP in centroacinar cells. Pancreozymin, caerulein, and the C-terminal octapeptide of pancreozymin inhibited the production of cyclic AMP observed with secretin of VIP, suggesting that the first three peptides were acting at a binding site different from the agonists, but coupled with the same adenylate cyclase. In acinar cells, secretin was able to exert slight ecbolic effects, and was also able to potentiate the effect of maximal concentrations of pancreozymin, caerulein, or the C-terminal octapeptide of pancreozymin. There was no simple correlation between amylase output and cyclic AMP levels, and copious amylase secretion was elicited even at control levels of cyclic AMP. Glucagon was neither an agonist nor an antagonist of any of the other polypeptides tested.

Amylases↗

Distribution of gastrointestinal hormones in the adaptive response after small bowel transplantation.

Enteroendocrine regulatory peptides may play an important role in the adaptation of small bowel mucosa, and it is likely that they act interdependently with neural and luminal stimuli. We assessed their action in rats by morphometric evaluation of enteroendocrine cells after heterotopic accessory small bowel transplantation (SBT), in which the graft is shunted off from the intestinal passage and is entirely deprived of neural connections, and after orthotopic SBT with normal intestinal passage. Sections of the jejunum and the ileum of the graft were immunostained with antibodies to cholecystokinin (CKK), neurotensin (NT) and vasoactive intestinal peptide (VIP). The amount and distribution of positive cells was assessed semiquantitatively. Three weeks after SBT in the heterotopic graft there was a marked decrease in CCK and NT positive cells and VIP positive fibres in the entire organ, compared with the controls. Histological examination revealed that villi and crypts had atrophied. After orthotopic SBT the number of CCK and NT positive cells increased and exceeded normal values by 20-40%. VIP positive fibres did not reach normal amounts. No mucosal atrophy was detected. These findings support the view that the intrinsic neurohormonal system is reestablished in the grafted small bowel and that enteroendocrine regulatory peptides may act as trophic factors that are responsible for adaptation after SBT.

Adaptation, Physiological↗

[Gastrointestinal hormones and operations for achalasia of the esophagus and sliding esophageal hiatal hernia: their surgical significance].

Experimental achalasia dogs produced with Deloyer's method showed higher resting pressure at the gastroesophageal junction and the increase in LES pressure in response to tetragastrin and cholecystokinin. Dose-response curve of the LES to each dose of tetragastrin in achalasia dog shifted to the left. Resting LES pressure in 11 patients with achalasia was 42.73 +/- 23.31 cm H2O. It increased significantly after intramuscular injection of 5 micrograms/kg of tetragastrin and fluoroscopic observation showed the tonic contraction of the lower esophagus and cardia. After the performance of Jekler-Lhotka operation, LES pressure decreased to lower values sufficient to prevent the gastroesophageal reflux. Comparing 5 kinds of hiatal herniorrhaphies in dogs, LES pressure increased postoperatively in the following order: Nissen, Belsey Mark IV, Stensrud, Hill and Harrington methods. Responses to tetragastrin increased after Nissen and Belsey Mark IV methods. In 12 out of 21 clinical cases of sliding esophageal hiatal hernia who had undergone Nissen-Rossetti method adding fundopexy and posterior gastropexy, preoperative esophageal manometry showed HPZ of 24.98 +/- 8.87 cm H2O in peak value and 5.1 +/- 3.46 cm in length. Seven cases showed the biphasic pattern and 5 cases showed the negative response to tetragastrin. Postoperative manometry showed HPZ of 31.42 +/- 18.46 cm H2O in peak value and 4.5 +/- 1.73 cm in length. One case showed the biphasic pattern and 3 cases showed the negative response to tetragastrin.

Animals↗

A novel bombesin receptor antagonist (2258U89), potently inhibits bombesin evoked release of gastrointestinal hormones from rats and dogs, in vitro and in vivo.

Several bombesin-receptor antagonists are available that inhibit secretory and growth effects of bombesin, in vitro. In the present study, we examined the effects of a new class of bombesin receptor antagonists (modified GRP(15-27) peptides, with D-Pro26 and D-Ala24 moieties), on bombesin mediated effects, in vivo and in vitro. Of the 10 different compounds tested, BW-10 or 2258U89 ([de-NH2)Phe19,D-Ala24,D-Pro26 psi(CH2NH)Phe27]-GRP(19-27)) was most potent towards inhibiting bombesin binding to rat pancreatic acinar cancer cells with an ID50 of 0.5 nM. BW-10 (1 and 10 nM) significantly inhibited the gastrin response to 1 nM bombesin, from isolated rat stomach, in vitro, in a dose-dependent fashion. BW-10 (10-100 nmol/kg) was equally effective at significantly inhibiting bombesin evoked gastrin release in anesthetized rats, in vivo. [D-Phe6]Bombesin(6-13)-propylamide (BIM), a member of another class of antagonists, reported previously to be the most potent antagonist, in vitro, on the other hand, enhanced bombesin provoked gastrin release in rats. The antagonistic effects of BIM, in vivo, may thus be more selective. Intravenous infusion of BW-10 (10 nmol/kg/h) partially depressed gastrin and pancreatic polypeptide and completely abolished insulin released in response to bombesin, in conscious dogs. These results suggest that BW-10 functions as one of the most potent bombesin receptor antagonists, in vitro and in vivo, which could potentially be used as a therapeutic compound in treatment of some human diseases.

Animals↗

Effects of four orally administered analogues of prostaglandin E1 and E2 on glucose tolerance and on the secretion of pancreatic and gastrointestinal hormones in man.

Oral glucose tolerance tests (75 g, 300 ml) were performed in 12 healthy volunteers, with prior administration of placebo, misoprostol (400 micrograms), rioprostil (300 micrograms), enprostil (70 micrograms), or nocloprost (200 micrograms), in a double-blind, randomized manner. None of the drugs significantly affected glucose tolerance, although with misoprostal some volunteers displayed an impaired glucose tolerance. Nocloprost was without effect on gastric inhibitory polypeptide (GIP) and did not influence insulin or C-peptide concentrations. Misoprostol and rioprostil reduced integrated incremental responses of GIP by 57% (P less than or equal to 0.001) and 45% (P less than or equal to 0.01), respectively, and both gave rise to an initial (approximately 10 min) delay of insulin and C-peptide responses, without a significant overall reduction in integrated incremental responses. Enprostil almost totally inhibited the GIP response (by 94%; P less than or equal to 0.001), delayed initial insulin and C-peptide responses, but reduced the integrated incremental C-peptide response (which corresponds to the overall release of insulin) by only 14% (P less than or equal to 0.05). Enprostil more substantially reduced the integrated incremental response of insulin by 36% (P less than or equal to 0.01), and also reduced the ratio of insulin and C-peptide incremental responses (P less than or equal to 0.001). In conclusion, prostaglandin E analogues which caused a reduction in GIP responses, and thereby disrupting the enteroinsular axis to varying degrees, delayed the time-course of insulin secretion without a significant impact on glucose tolerance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Appetite, food intake, and plasma concentrations of cholecystokinin, ghrelin, and other gastrointestinal hormones in undernourished older women and well-nourished young and older women.

Aging is associated with a reduction in appetite and food intake, predisposing to protein-energy malnutrition. The causes of this "anorexia of aging" are largely unknown. To investigate possible contributions of enhanced satiating effects of cholecystokinin (CCK) and reduced stimulation of food intake by ghrelin, eight undernourished older women [age, 80.4 +/- 2.6 yr; body mass index (BMI), 16.9 +/- 0.57 kg/m(2)], eight well-nourished older women (age, 77 +/- 0.9 yr; BMI, 23.7 +/- 0.8 kg/m(2)), and eight well-nourished young women (age, 22 +/- 1.3 yr; BMI, 20.5 +/- 0.4 kg/m(2)), in randomized order, ate on 1 d a 280-kCal preload and on the other no preload, 90 min before an ad libitum meal. At baseline the undernourished, but not the well-nourished, older subjects were less hungry (P < 0.05) than young subjects. Before and after the preload, plasma CCK levels were higher (P < 0.05) in the older than young subjects, with no difference between the older groups. Plasma ghrelin concentrations were higher in the undernourished than both well-nourished groups and decreased similarly after the preload in all groups. The preload suppressed food intake in the well-nourished older and young subjects (P < 0.05), but was without effect in the undernourished old. These observations suggest that reduced basal hunger, rather than increased meal-induced satiety, contributes to the anorexia of aging and that changes in CCK and ghrelin are unlikely to be responsible.

Aged↗

Effect of euglycaemic hyperinsulinaemia on gastric emptying and gastrointestinal hormone responses in normal subjects.

Several studies have shown that hyperglycaemia slows gastric emptying in normal subjects and patients with diabetes mellitus but whether hyperinsulinaemia per se has an effect remains debatable. In the present study we have assessed the effect of hyperinsulinaemia on gastric emptying of a solid and liquid meal in normal subjects. Ten men were studied three times in random order. After an overnight fast, subjects were infused with 0.9% NaCl on two occasions and on the third with insulin, at 40 mU x m(-2) x min(-1) with 20% glucose simultaneously to maintain euglycaemia. Steady-state glucose infusion rate was ensured before the subjects ate a standard meal of a pancake labelled with 99mTc and milkshake labelled with (111)In-DTPA. Gamma-scintigraphic images were then obtained every 20 min for the next 3 h. There were no significant differences between the mean half-emptying times (T50) of the solid and liquid during the two saline infusions (129.6 +/- 28.5 vs 128.4 +/- 23.8 min for the solid and 25.4 +/- 7.0 vs 34.7 +/- 18.0 min for the liquid, mean +/- SD). Hyperinsulinaemia delayed both solid (mean T50 149.6 +/- 30.7, p = 0.031) and liquid emptying (mean T50 39.8 +/- 13.9, p = 0.042). There were no significant differences in the cholecystokinin and glucagon-like peptide 1 responses to the meal during either saline or insulin infusions. There was a tendency towards a greater insulin response to the meal during the hyperinsulinaemic study. Thus, hyperinsulinaemia delayed emptying of both the solid and liquid components of the meal.

Adult↗